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Loss of function of the new interferon IFN-λ4 may confer protection from hepatitis C

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Attempts to elucidate the mechanism underpinning the genetic association between IFNL3, previously called IL28B, and clearance of hepatitis C virus have, by and large, been unsuccessful. A study in this issue suggests that a new gene, IFNL4, may be responsible.

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Figure 1: IFNL4 genomic location and signaling.

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Authors and Affiliations

  1. David Booth is at the Institute for Immunology and Allergy Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia.,

    David Booth

  2. Jacob George is at the Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney, Sydney, New South Wales, Australia.,

    Jacob George

Authors
  1. David Booth
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  2. Jacob George
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Corresponding author

Correspondence to Jacob George.

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Competing interests

D.B. and J.G. have filed patent applications in Australia and the United States for use of the IL28B gene region to predict drug response.

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Booth, D., George, J. Loss of function of the new interferon IFN-λ4 may confer protection from hepatitis C. Nat Genet 45, 119–120 (2013). https://doi.org/10.1038/ng.2537

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